Effects of chronic noradrenaline on the nitric oxide pathway in human endothelial cells

T. Bachetti, L. Comini, L. Agnoletti, P. Pedersini, G. Gaia, A. Cargnoni, M. Bellet, S. Curello, R. Ferrari

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Altered endothelium-dependent vasodilation has been observed in congestive heart failure (CHF), a disease characterized by a sustained adrenergic activation. The purpose of our study was to test the hypothesis that chronically elevated catecholamines influence the nitric oxide (NO) pathway in the human endothelium. Human umbilical vein endothelial cells (HUVEC) were exposed for 7 days to a concentration of noradrenaline (NA,1 ng/mL) similar to that found in the blood of patients with CHE Kinetics of endothelial constitutive NO synthase (ecNOS) and inducible NO synthase (iNOS) activity, measured by [3H]L arginine to [3H]L-citrulline conversion, and protein expression of ecNOS and iNOS, assessed by Western blot analysis, were unaffected by chronic NA treatment. Furthermore, no changes in subcellular fraction-associated ecNOS were found; this indirectly shows that chronic NA did not cause phosphorylation of the enzyme. Moreover, [3H]L-arginine transport through the plasma membrane was conserved in chronically NA-treated cells. The data demonstrate that prolonged in vitro exposure to pathologic CHF-like NA does not affect the L-arginine: NO pathway in human endothelial cells.

Original languageEnglish
Pages (from-to)250-256
Number of pages7
JournalBasic Research in Cardiology
Issue number4
Publication statusPublished - Aug 1998


  • Endothelial cells
  • Nitric oxide
  • Nitric oxide synthase
  • Noradrenaline

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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